to thrive and have a series of symptoms that cause abnormalities in the joints, hair, skin, eyes, and face. Most who have the disease only live to about age 13. Although the term progeria applies strictly speaking to all diseases characterized by premature aging symptoms, and is often used as such, it is often applied specifically in reference to Hutchinson–Gilford progeria syndrome (HGPS). Children diagnosed with HGPS develop prominent facial features such as a small face, thin lips, small chin, and protruding ears. Although progeria can cause physical abnormalities on a child, it does not impact their motor skills or intellectual advancement. Those who have HGPS are prone to suffer from neurological and cardiovascular disorders. HGPS is caused by a point mutation in the gene that encodes lamin A protein. Lamin A promotes genetic stability by maintaining levels of proteins that have key roles in non-homologous end joining and homologous recombination. Mouse cells deficient for maturation of prelamin A show increased DNA damage and chromosome aberrations and have increased sensitivity to DNA damaging agents. In HGPS, the inability to adequately repair DNA damages due to defective A-type lamin may cause aspects of laminopathy-based premature aging. Werner Syndrome Werner syndrome, also known as "adult progeria", is another single-gene genetic disease. it is caused by a mutation in the wrn gene. It affects about 1 in 200,000 people in the United States. This syndrome starts to affect individuals during the teenage years, preventing teens from growing at puberty. There are four common traits of Werner's syndrome: cataracts in both eyes, changes in skin similar to scleroderma, short stature, and early graying and loss of hair. Once the individual reaches the twenties, there is generally a change in hair color, skin, and voice. The average life expectancy of someone with this disease is around 46 years. This condition can also affect the weight distribution between the arms, legs, and torso. Those who have Werner syndrome are at an increased risk for cataracts, type 2 diabetes, different types of cancers, and atherosclerosis. The finding that WRN protein interacts with DNA-PKcs and the Ku protein complex, combined with evidence that WRN deficient cells produce extensive deletions at sites of joining of non-homologous DNA ends, suggests a role for WRN protein in the DNA repair process of non-homologous end joining. WRN protein also appears to play a role in resolving recombination intermediate structures during homologous recombinational